Pathophysiological Mechanisms Underlying Neurodegenerative Disorders

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Neuropharmacology and Neuropathology".

Deadline for manuscript submissions: closed (5 October 2023) | Viewed by 2784

Special Issue Editor


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Guest Editor
Medical Physiology, Mansoura Faculty of Medicine, Mansoura, Egypt
Interests: neurosciences: epilepsy, Parkinsonism, autism, deep brain stimulation; stem cell research and regenerative medicine; oxidative stress and pathways of oxidant and antioxidant systems such as Nrf2/HO1 pathway; natural plant extracts such as stevia R, palm date fruits and seed extracts

Special Issue Information

Dear Colleagues,

Neurodegenerative disorders (NDD) are a group of diseases characterized by selective dysfunction and progressive loss of neurons, glial cells, and their networks in different parts of the nervous system. Patients with NDD display progressive cognitive loss and/or motor dysfunction as a consequence; for instance, Alzheimer's disease (AD) is characterized by a decrease in cognitive function, whereas amyotrophic lateral sclerosis (ALS), Parkinson's disease (PD), and Huntington's disease (HD) all exhibit motor deficits (HD). Despite the wide variety of causes of NDD, several research groups have demonstrated that they share common pathways such as the accumulation of insoluble protein aggregates, apoptosis, necrosis, excitotoxicity, and neuroinflammation. Other significant contributors to neurodegeneration include diminished autophagy/lysosomal activity, downstream oxidative stress, and mitochondrial dysfunction. Animal models are effective research tools for figuring out the causes and molecular mechanisms of neurodegenerative diseases as well as discovering new therapeutic agents. This Special Issue aims to present the latest updates on the molecular mechanisms of neurodegenerative diseases in both animal and human studies. 

Prof. Dr. Abdelaziz M. Hussein
Guest Editor

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Keywords

  • neurodegeneration
  • neuroinflammation
  • excitotoxicity
  • neuronal and neuroglial cell deaths
  • mitochondrial dysfunctions
  • autophagy

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Published Papers (1 paper)

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Research

17 pages, 5195 KiB  
Article
Vanillic Acid Ameliorates Demyelination in a Cuprizone-Induced Multiple Sclerosis Rat Model: Possible Underlying Mechanisms
by Sally M. Safwat, Mahmoud El Tohamy, Moutasem Salih Aboonq, Amaal Alrehaili, Ahmad A. Assinnari, Abdulrahman S. Bahashwan, Ahmed A. ElGendy and Abdelaziz M. Hussein
Brain Sci. 2024, 14(1), 12; https://doi.org/10.3390/brainsci14010012 - 22 Dec 2023
Cited by 6 | Viewed by 2161
Abstract
Objective: To investigate the effect of vanillic acid (VA) on a Cuprizone (Cup) demyelinating rat model and the mechanisms behind such effect. Methods: Thirty adult male Sprague Dawley (SD) rats were randomly divided into three groups: control, Cuprizone, and VA groups. Cuprizone was [...] Read more.
Objective: To investigate the effect of vanillic acid (VA) on a Cuprizone (Cup) demyelinating rat model and the mechanisms behind such effect. Methods: Thirty adult male Sprague Dawley (SD) rats were randomly divided into three groups: control, Cuprizone, and VA groups. Cuprizone was administrated at a dose of 450 mg/kg per day orally via gastric gavage for 5 weeks. The nerve conduction velocity (NCV) was studied in an isolated sciatic nerve, and then the sciatic nerve was isolated for histopathological examination, electron microscope examination, immunohistochemical staining, and biochemical and PCR assay. The level of IL17 was detected using ELISA, while the antioxidant genes Nrf2, HO-1 expression at the level of mRNA, expression of the myelin basic protein (MBP), interferon-gamma factor (INF)-γ and tumor necrosis factor (TNF)-α, and apoptotic marker (caspase-3) were measured using immunohistochemistry in the sciatic nerve. Results: There was a significant reduction in NCV in Cup compared to normal rats (p < 0.001), which was markedly improved in the VA group (p < 0.001). EM and histopathological examination revealed significant demyelination and deterioration of the sciatic nerve fibers with significant improvement in the VA group. The level of IL17 as well as the expression of INF-γ and caspase-3 were significantly increased with a significant reduction in the expression of MBP, Nrf2, and HO-1 in the sciatic nerve (p < 0.01), and VA treatment significantly improved the studied parameters (p < 0.01). Conclusion: The current study demonstrated a neuroprotective effect for VA against the Cup-induced demyelinating rat model. This effect might be precipitated by the inhibition of inflammation, oxidative stress, and apoptosis. Full article
(This article belongs to the Special Issue Pathophysiological Mechanisms Underlying Neurodegenerative Disorders)
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